123 research outputs found

    Current Options for Visualization of Local Deformation in Modern Shape Analysis Applied to Paleobiological Case Studies

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    In modern shape analysis, deformation is quantified in different ways depending on the algorithms used and on the scale at which it is evaluated. While global affine and non-affine deformation components can be decoupled and computed using a variety of methods, the very local deformation can be considered, infinitesimally, as an affine deformation. The deformation gradient tensor F can be computed locally using a direct calculation by exploiting triangulation or tetrahedralization structures or by locally evaluating the first derivative of an appropriate interpolation function mapping the global deformation from the undeformed to the deformed state. A suitable function is represented by the thin plate spline (TPS) that separates affine from non-affine deformation components. F, also known as Jacobian matrix, encodes both the locally affine deformation and local rotation. This implies that it should be used for visualizing primary strain directions (PSDs) and deformation ellipses and ellipsoids on the target configuration. Using C = FTF allows, instead, one to compute PSD and to visualize them on the source configuration. Moreover, C allows the computation of the strain energy that can be evaluated and mapped locally at any point of a body using an interpolation function. In addition, it is possible, by exploiting the second-order Jacobian, to calculate the amount of the non-affine deformation in the neighborhood of the evaluation point by computing the body bending energy density encoded in the deformation. In this contribution, we present (i) the main computational methods for evaluating local deformation metrics, (ii) a number of different strategies to visualize them on both undeformed and deformed configurations, and (iii) the potential pitfalls in ignoring the actual three-dimensional nature of F when it is evaluated along a surface identified by a triangulation in three dimensions

    Cardiovascular toxicity from therapies for light chain amyloidosis

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    : Amyloid light-chain (AL) amyloidosis is a hematological disorder characterized by abnormal proliferation of a plasma cell clone producing monoclonal free light chains that misfold and aggregate into insoluble fibrils in various tissues. Cardiac involvement is a common feature leading to restrictive cardiomyopathy and poor prognosis. Current first-line treatments aim at achieving hematological response by targeting the plasma cell clones, and these have been adapted from multiple myeloma therapy. Patients with AL amyloidosis often exhibit multiorgan involvement, making them susceptible to cancer therapy-related cardiovascular toxicity. Managing AL amyloidosis is a complex issue that requires enhanced knowledge of the cardio-oncological implications of hematological treatments. Future research should focus on implementing and validating primary and secondary prevention strategies and understanding the biochemical basis of oncological therapy-related damage to mitigate cardiovascular toxicity

    What Is Hidden Behind Inferior Negative T Waves: Multiple Cardiac Glomangiomas

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    Abstract Negative T waves in the inferior leads in an asymptomatic 17-year-old female patient prompted a diagnostic evaluation disclosing the presence of multiple cardiac glomangiomas. The combination of different imaging modalities (echocardiography, magnetic resonance, and positron emission tomography/computed tomography) and myocardial biopsy was crucial to establishing the correct diagnosis. (Level of Difficulty: Advanced.

    Cardiovascular disease and COVID-19 : les liaisons dangereuses

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    Patients with cardiovascular risk factors or established cardiovascular disease have an increased risk of developing coronavirus disease 19 and have a worse outcome when infected, but translating this notion into effective action is challenging. At present it is unclear whether cardiovascular therapies may reduce the likelihood of infection, or improve the survival of infected patients. Given the crucial importance of this issue for clinical cardiologists and all specialists dealing with coronavirus disease 19, we tried to recapitulate the current evidence and provide some practical recommendations

    Cardiovascular toxicity from therapies for light chain amyloidosis

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    Amyloid light-chain (AL) amyloidosis is a hematological disorder characterized by abnormal proliferation of a plasma cell clone producing monoclonal free light chains that misfold and aggregate into insoluble fibrils in various tissues. Cardiac involvement is a common feature leading to restrictive cardiomyopathy and poor prognosis. Current first-line treatments aim at achieving hematological response by targeting the plasma cell clones, and these have been adapted from multiple myeloma therapy. Patients with AL amyloidosis often exhibit multiorgan involvement, making them susceptible to cancer therapy-related cardiovascular toxicity. Managing AL amyloidosis is a complex issue that requires enhanced knowledge of the cardio-oncological implications of hematological treatments. Future research should focus on implementing and validating primary and secondary prevention strategies and understanding the biochemical basis of oncological therapy-related damage to mitigate cardiovascular toxicity

    From Smart Apes to Human Brain Boxes. A Uniquely Derived Brain Shape in Late Hominins Clade

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    Modern humans have larger and more globular brains when compared to other primates. Such anatomical features are further reflected in the possession of a moderately asymmetrical brain with the two hemispheres apparently rotated counterclockwise and slid anteroposteriorly on one another, in what is traditionally described as the Yakovlevian torque. Developmental disturbance in human brain asymmetry, or lack thereof, has been linked to several cognitive disorders including schizophrenia and depression. More importantly, the presence of the Yakovlevian torque is often advocated as the exterior manifestation of our unparalleled cognitive abilities. Consequently, studies of brain size and asymmetry in our own lineage indirectly address the question of what, and when, made us humans, trying to trace the emergence of brain asymmetry and expansion of cortical areas back in our Homo antecedents. Here, we tackle this same issue by studying the evolution of human brain size, shape, and asymmetry on a phylogenetic tree including 19 apes and Homo species, inclusive of our fellow ancestors. We found that a significant positive shift in the rate of brain shape evolution pertains to the clade including modern humans, Neanderthals, and Homo heidelbergensis. Although the Yakovlevian torque is well evident in these species and levels of brain asymmetry are correlated to changes in brain shape, further early Homo species possess the torque. Even though a strong allometric component is present in hominoid brain shape variability, this component seems unrelated to asymmetry and to the rate shift we recorded. These results suggest that changes in brain size and asymmetry were not the sole factors behind the fast evolution of brain shape in the most recent Homo species. The emergence of handedness and early manifestations of cultural modernity in the archeological record nicely coincide with the same three species sharing the largest and most rapidly evolving brains among all hominoids

    Valve disease in cardiac amyloidosis: an echocardiographic score

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    Cardiac amyloidosis (CA) may affect all cardiac structures, including the valves. From 423 patients undergoing a diagnostic workup for CA we selected 2 samples of 20 patients with amyloid transthyretin (ATTR-) or light-chain (AL-) CA, and age- and sex-matched controls. We chose 31 echocardiographic items related to the mitral, aortic and tricuspid valves, giving a value of 1 to each abnormal item. Patients with ATTR-CA displayed more often a shortened/hidden and restricted posterior mitral valve leaflet (PMVL), thickened mitral chordae tendineae and aortic stenosis than those with AL-CA, and less frequent PMVL calcification than matched controls. Score values were 15.8 (13.6-17.4) in ATTR-CA, 11.0 (9.3-14.9) in AL-CA, 12.8 (11.1-14.4) in ATTR-CA controls, and 11.0 (9.1-13.0) in AL-CA controls (p = 0.004 for ATTR- vs. AL-CA, 0.009 for ATTR-CA vs. their controls, and 0.461 for AL-CA vs. controls). Area under the curve values to diagnose ATTR-CA were 0.782 in patients with ATTR-CA or matched controls, and 0.773 in patients with LV hypertrophy. Patients with ATTR-CA have a prominent impairment of mitral valve structure and function, and higher score values. The valve score may help identify patients with ATTR-CA among patients with CA or unexplained hypertrophy

    Pathophysiological Rationale and Clinical Evidence for Neurohormonal Modulation in Heart Failure with Preserved Ejection Fraction

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    Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome resulting from the interaction between cardiac diseases, comorbidities and ageing. HFpEF is characterised by the activation of neurohormonal axes, namely of the renin-angiotensin-aldosterone system and the sympathetic nervous system, although to a lesser extent compared with heart failure with reduced ejection fraction. This provides a rationale for neurohormonal modulation as a therapeutic approach for HFpEF. Nonetheless, randomised clinical trials have failed to demonstrate a prognostic benefit from neurohormonal modulation therapies in HFpEF, with the sole exception of patients with left ventricular ejection fraction in the lower range of normality, for whom the American guidelines suggest that such therapies may be considered. In this review, the pathophysiological rationale for neurohormonal modulation in HFpEF is summarised and the clinical evidence on pharmacological and nonpharmacological approaches backing current recommendations discussed

    Left ventricular wall thickness and severity of cardiac disease in women and men with transthyretin amyloidosis

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    Aims: Cardiac amyloidosis (CA) is due to a deposition of amyloid fibrils in the heart causing an increase in wall thickness. A left ventricular (LV) wall thickness ≥12 mm plus at least one red flag should raise the suspicion of CA. As normal values of LV wall thickness are lower in women, the adoption or the same cut-off values for men and women could lead to underdiagnosis or delayed diagnosis in women. We investigated the relationship between LV wall thickness and the severity of cardiac involvement in women and men with transthyretin (ATTR) CA. Methods and results: We evaluated 330 consecutive patients diagnosed with ATTR-CA at three centres (Pisa, n = 232; Brescia, n = 69; Trieste, n = 29). Interventricular septum (IVS) and posterior wall (PW) thickness values were lower in women (n = 53, 16%) than men, but most differences were abolished when indexing by body surface area (BSA), height, or height, suggesting similar disease severity when accounting for the smaller body size of women. PW thickness indexed for height was even higher in women. We also searched for correlations between IVS and PW thickness and other indicators of the severity of cardiac disease. IVS values indexed by height displayed tighter associations with N-terminal pro-B-type natriuretic peptide values than non-indexed IVS values. Similarly, indexed values displayed closer relationships with relative wall thickness, E/e' ratio, and tricuspid annular plane systolic excursion. Conclusions: Indexed LV wall thickness values, particularly by height, reflect more accurately the severity of cardiac involvement than non-indexed values
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